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Altered expression of KCNK9 in colorectal cancers
Author(s) -
KIM CHANG JAE,
CHO YONG GU,
JEONG SEONG WHAN,
KIM YOUNG SIL,
KIM SU YOUNG,
NAM SUK WOO,
LEE SUG HYUNG,
YOO NAM JIN,
LEE JUNG YOUNG,
PARK WON SANG
Publication year - 2004
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2004.apm1120905.x
Subject(s) - colorectal cancer , cancer research , medicine , cancer , immunohistochemistry , pathology , biology , oncology
K + channels have been reported to be involved in the proliferation of many types of cells, including some human carcinoma and tumor cell lines. KCNK9, a TASK channel, is amplified and overexpressed in several types of human cancer. In the present study, we examined the expression and somatic mutations of KCNK9 in 124 colorectal cancers by immunohistochemistry using tissue microarray and PCR‐SSCP. Immunopositivity was observed in 57 (46.0%) of 124 colorectal cancers. Clinically, KCNK9 was immunopositive in 4 (30.7%) of 13 cases which were stage A, 26 (55.3%) of 47 which were stage B, 23 (41.1%) of 56 which were stage C, and 4 (50%) of 8 which were stage D. Statistically, KCNK9 protein expression was not related to tumor stage (Bartholomew test, p>0.05) and lymph node metastasis (Chi‐Square test, p=0.8338). In the mutation study of the KCNK9 gene, we found only one sequence variation (ACG→ACC, Thr→Thr) at codon 170 both in corresponding normal and tumor DNAs. These results indicate that overexpression rather than mutation of the KCNK9 gene may contribute to the development of colorectal cancers and suggest that the development of KCNK9‐targeted agents may provide new possibilities in the treatment of colorectal cancer.